Kilpatrick I C, Starr M S, Fletcher A, James T A, MacLeod N K
Exp Brain Res. 1980;40(1):45-54. doi: 10.1007/BF00236661.
Unilateral stereotaxic microinjection of muscimol into the caudal region of the substantia nigra (SN) evoked tight, dose-related contralateral locomotor asymmetry and stereotypy. These behaviours were partially attenuated by various pretreatments, including 6-hydroxydopamine lesions of the nigrostriatal dopamine pathway, intraperitoneal (i.p.) haloperidol, and inhibition of thalamic GABA-transaminase activity by local intrathalamic injection of ethanolamine-O-sulphate. Electrolytic or kainic acid lesions of the medial thalamic nuclei (MTN) partially reduced the contraversive rotation to intranigral muscimol, and completely abolished the similar behaviour elicited by apomorphine (25 microgram) injected into the ipsilateral caudate nucleus. Contraversive turning to intranigral muscimol was completely inhibited by kainic acid lesions of the ipsilateral SN, but potentiated by intrahalamic injection of picrotoxin. Muscimol (40 ng--4 microgram) administered to the MTN complex in one hemisphere stimulated rats to move in ipsilateral circles that were unaffected by haloperidol. The results of these behavioural experiments suggest that the nigrostriatal dopamine pathway, the nigrothalamic projection and possibly other non-dopaminergic SN efferents all play important roles in mediating the influences of the SN on motor and stereotyped behaviours. Disruption of the nigrothalamic pathway following electrical or chemical injury to the SN was accompanied by falls in GABA and its synthesising enzyme in the corresponding MTN. These data, together with the findings of our electrophysiological study presented in the following paper, are consistent with the nigrothalamic system having a GABAergic inhibitory function.
向黑质(SN)尾侧区域单侧立体定向微量注射蝇蕈醇可诱发紧密的、剂量相关的对侧运动不对称和刻板行为。这些行为可被多种预处理部分减弱,包括黑质纹状体多巴胺通路的6-羟基多巴胺损伤、腹腔注射氟哌啶醇,以及通过丘脑内局部注射乙醇胺-O-硫酸盐抑制丘脑GABA转氨酶活性。内侧丘脑核(MTN)的电解或 kainic 酸损伤可部分减少对黑质内蝇蕈醇的对侧旋转,并完全消除向同侧尾状核注射阿扑吗啡(25微克)所引发的类似行为。向同侧SN注射 kainic 酸可完全抑制对黑质内蝇蕈醇的对侧旋转,但向丘脑内注射印防己毒素可增强这种旋转。向一侧半球的MTN复合体注射蝇蕈醇(40纳克 - 4微克)可刺激大鼠向同侧转圈,且不受氟哌啶醇影响。这些行为实验结果表明,黑质纹状体多巴胺通路、黑质丘脑投射以及可能的其他非多巴胺能SN传出纤维在介导SN对运动和刻板行为的影响中均起重要作用。SN受到电损伤或化学损伤后黑质丘脑通路的破坏伴随着相应MTN中GABA及其合成酶的减少。这些数据,连同我们在下一篇论文中呈现的电生理研究结果,与黑质丘脑系统具有GABA能抑制功能一致。